Transcription

Jeff Maglin: It’s my pleasure to introduce our speaker, Rob DiBlasi. Rob is a research and QI manager, and respiratory therapy principle investigator at Seattle Children’s Research Institute from Seattle, Washington. He’s a registered respiratory therapist, neonatal pediatric specialist, and a fellow of the American Association of Respiratory Care. Rob has more than 20 years of respiratory bedside experience and close to 20 years in respiratory research. He has authored eight textbook chapters, 31 published articles, and 60 abstracts in respiratory care, and has received 12 grants for his research. His special interests include invasive and noninvasive ventilation and drug delivery in neonates and pediatrics. Rob is a frequently invited presenter at national, regional, and state respiratory and medical conferences both in the United States and internationally. He has been awarded on four separate occasions for his work. In 2012 was named the AARC neonatal pediatrics specialty practitioner of the year. I’d like to welcome Rob and I’ll now hand the controls over to him.

Rob DiBlasi: Thank you, Jeff, and good morning everybody. I appreciate all of you for tuning in. I’m really looking forward to this. I’ve been working on the bronchiolitis pathways for several years, and when Jeff approached me and asked me to kind of speak to all of you on our approach at Seattle Children’s Hospital, I was pretty excited. I have to say that respiratory management and bronchiolitis is a major part of any neonatal pediatric respiratory therapist, I have been actively involved in respiratory management guidelines for bronchiolitis at Seattle Children’s Hospital. I’m super excited to share some of our management guidelines with all of you, but especially to go through and look at all of the available evidence, and kind of rate that based on the therapies that we’re providing to infants with bronchiolitis.

I think this is timely because we’re starting to see kids that are coming into the hospital now, and we’ve seen a couple of kids with rhino entero, we’re starting to see some RSV coming into our hospital wards, and so it’s especially timely that we have these discussions about bronchiolitis, and how that impacts the care that you provide as respiratory therapists, as nurses, as physicians.

But I especially want to be able to thank Vapotherm for not only providing us with the opportunity to have these informed discussions. Sometimes it’s impossible to be able to have these discussions without industry support, but especially Vapotherm. I’d like to thank them, and thank Jeff Maglin for completely going out of his way and spending countless hours to make sure that this happens.

Without any further ado, we’re going to move through our presentation. As Jeff mentioned before, they’re not actually able to support any of our clinical guidelines. They are not a reference company for clinical management. This is being sponsored by Vapotherm. I will add, also, that any of the specific guidelines that we mention in this presentation, please take these, use them as much as you’d like. I’ll provide you with a PDF of our bronchiolitis management strategies, but also realize that there was a lot of time and effort that went into all of this. Please use it anyway you want, but as a medical disclaimer we’re not solely responsible for anything that may occur as a result of using our management guidelines.

In fact, working in the QI world, I typically will branch out to all of my friends and talk to people at multiple institutions to find out what they’re doing with regard to management of bronchiolitis, because we may cover the majority of things, and we may review every paper that’s out there, but there are some things that could be particularly, they could be updated.

These are some of the objectives that we’re going to talk about. We’re going to talk about the pathophysiology of bronchiolitis infection. I think this one is fairly compelling, because it’s very different from a lot of other respiratory diseases. It encompasses a large number of different viral pathogens, and it’s interesting how this disease is actually spread. It’s also interesting that this disease could be confined to the upper respiratory section of the lungs, but in those kids that are at greatest risk this viral event could actually make its way down into the lungs, and that could wreak havoc, and create a severe obstructive disease that could result in severe respiratory failure. That’s why it’s important that I think that we start from square one and identify those patients who are at high risk for this infection.

I think as long as we know as therapists, and nurses, and docs what the underlying pathophysiology entails, then we can understand when a patient’s condition is changing, and how we need to intervene in order to kind of correct their path, and make it so that they don’t have to be admitted to the ICU, or be subjected to potentially injurious invasive ventilation. We’re going to cover all those factors today.

We’re going to talk about the evidence related to the effectiveness of oxygen, specialty gases, which include mostly heliox gas, and we’ll talk about aerosolized medications, airway clearance, all things that we would typically have in our armamentarium to use in patients that are affected with bronchiolitis. Now, is there a lot of high-level evidence to support using these interventions? Well, we’re going to talk about that, and in the standard care of bronchiolitis, we may be limited to only using a few different things whereas as they get sicker we may want to try to pull things from our armamentarium and implement those for those kids that are most critical.

We’ll talk about some of the physiologic benefits related to nasal CPAP, NIPPV, and high-flow nasal cannula. We’ve learned a lot from our friends in the neonatal intensive care unit as of late. We’d say that it’s easy to say that about 70% of all babies that are supported in the NICU nowadays are done so with noninvasive ventilation, and there’s lesser use of invasive ventilation, so we’ve learned a lot from them, and we’re beginning to implement a lot of these strategies in patients with bronchiolitis.

We’ll talk about our evidence based management guidelines in patients effected with bronchiolitis. Again, branch out, benchmark, talk to other people, learn what they’re doing. When we look at epidemiology, it’s really a very interesting disease. Bronchiolitis basically means injury, inflammation, mucus plugging, bronchoconstriction in the bronchial tubes. This is a disease that affects primarily infants less than two years of age. In us, if we get infected with RSV, it’s very unlikely that we’re going to be affected with a true, full-on bronchitis. We may get an upper respiratory infection, mild low-grade fever. We may cough and some of us may go on to develop a little bit of a bronchitis, but in babies, because their airways are smaller, because the nasal airway resistance accounts for approximately two thirds of the total respiratory system resistance, those babies are at much greater risk for developing high work of breathing as a result of this acute infection.

With that being said, some of these babies may look worse than they really are, primarily because their nasal airway resistance is so high, they get a stuffy nose, they’re obligated to breathe through their nose in most cases, especially in the smaller infants, and so they have a tendency to look worse. Now, those are kids that we may just go in and suction and they look so much better, but that’s not to say that that disease is limited to their upper airway. That disease can migrate down into those distal bronchioles and create havoc. So this is a serious respiratory tract infection that impacts a lot of babies, a lot of infants worldwide. We oftentimes focus on our rates of hospitalization and deaths here in the United States, and the hospitalization rates are through the roof. It’s one of the number one reasons why children less than five years of age are admitted to the hospital.

The majority of the infants, by the age of one, are actually infected with RSV disease, but that doesn’t mean that they’re all going to get super sick. So in the United States, we see about 125,000. New numbers support maybe even higher hospitalization rates per year, maybe double that at a number of different institutions that have published recently. That only accounts for about 450 deaths, and most of those deaths occur in kids that have some chronic underlying condition. And so …

We got a little bit of feedback there, Jeff.

Jeff Maglin: Yes, I have it all muted on this side, I’ll take a look and see if there’s someone who came on that I need to mute as well. I would just ask everyone else on the phone to make sure you’re muted.

Rob DiBlasi: Excellent, thank you. But up to this point, everyone’s been able to hear me okay?

Good.

Okay, so the one thing that we need to focus on is, let’s not be selfish here. We live in the United States. Most of you live in the United States where healthcare is available and we have lots of different things that we can throw at kids with this disease. But outside of the United States, and I have traveled to some of these places that include India, Egypt, I’m going to South America this week. I will say that there are many kids that will go on to develop severe RSV infections, bronchiolitis, or there’s a whole host of other viral pathogens that can cause this. They will go on to develop severe pneumonia. There are millions of deaths outside of the US every year in children less than five years of age that are attributable to viral respiratory infection.

With that in mind, there’s a lot that I think that we can all learn together. Now, in those resource-limited settings, they may not have the available treatment options. Here in the United States, we’ve got everything. We’ve got CBT, we’ve got albuterol, we’ve got steroids. We’ve got all these things, and I think that the fact that we are able to throw all these things at patients or provide these different types of innovations to patients, this has resulted in billions of healthcare dollars that are spent annually for those babies that are infected with this viral disease.

Most of the kids, again, this is not going to affect people outside of two years age as much. I mean, you may see that they get a severe upper respiratory infection, but the bronchitis is not as severe. In the majority of babies that are born, and a lot of these babies that are breastfeeding and the babies in the first six months or so, they’re not likely to get infected because they carry with them antibodies from their moms who have previously been infected. So at least the severity of disease in those babies is not super high. It’s in those babies that have chronic lung disease or have congenital heart disease or neuromuscular weakness, or those babies that may be affected by cystic fibrosis or they have a recurrent aspiration pneumonitis, tracheal-esophageal fistula, neurological conditions that may impair their ability to remove secretions from the airways. Those are the kids that are at greater risk.

So we’re seeing lots of chronic kids nowadays that are admitted back into the PICU, and these may be some of the kids that we took care of in the NICU. Some of them may be tracheotomized, some of them may be on chronic ventilation, but the second they get this disease, they’re more likely to come back into the hospital. But it’s also interesting that once patients are in the hospital, they may come into the hospital free of this virus, it is a very common form of nosocomial pneumonia or nosocomial infection.

Health care providers are the ones that are most likely to spread this to patients who are in the hospital, so that’s why it’s especially important to wash your hands. But also to talk to family members, because there are certain patients that are at risk that are immunocompromised, or those who are around passive cigarette smoking, where they’re breathing smoke off of parents’ clothing, and the mucociliary escalator has become ineffective, the cilia laying down, and they’re more likely to have the viral replication and worsening disease in those cases, because it gets further down into the lung, so super important.

I think that the clinical progression of this disease is super, super interesting, and this is what the RSV virus looks like under microscopy. Again, the RSV, respiratory syncytial virus accounts for 50 to 80% of all the infections, and I will mention that co-infection rates with bacterial pathogens really is fairly low. I think it’s upwards of 30%. Obviously, those kids with chronic disease are going to be more likely to develop some of those co-infections, and I think that’s why we probably don’t do as many x- rays and we don’t prescribe as many antibiotics. But for the most part, this is a self-limiting disease. It can be caused by human metapneumovirus, rhinovirus, coronavirus, parainfluenza, lots of different things that can bring this on.

The way that it is transmitted to patients, it’s fairly interesting because the majority of infections that occur are through droplets, but I think we’re getting better with putting our hands over our mouths when we sneeze. Those droplets actually can be transmitted ocularly, they can be transmitted through the nasal mucosa, hand to hand, and then you take your hand and you put it up against your eye, or your nose, your buccal mucosa, and basically the child will kind of ingest or inhale those droplets. For the most part, if we look at the lung lining and we look at the bronchial lumen, the epithelial cells, the pseudo ciliated columnar epithelial cells are pretty prevalent all the way down through the airways, and they’re responsible for moving all of the junk out of the lungs. However, if we inhale those droplets or we put those droplets up against our eyes or our mouth and they tend to get into the nasal airway epithelial cells, it takes about four to six days, and that’s when we start to see that the fever comes on, there’s some congestion, rhinorrhea, that the kid’s more irritable, that they’re not really feeding as well, because any kid that’s in respiratory distress really doesn’t want to be taking their bottle feeds or taking their breast feeds. So after two to three days of the onset of the upper respiratory tract infection, we start to see in those individuals that are going to progress with this disease, we start to see that they have lower respiratory tract or bronchiolitis manifestations. And so this typically will result in babies who are coughing. They become tachypneic, they may have evidence of cyanosis, they have wheezing and maybe we’ll see some hyperinflation in these kids, because we get the cells that end up proliferating and sloughing off into the airway.

So that’s what it looks like here, where in a kid who has pretty advanced disease, the virus gets into the nasal epithelial airway cells. It replicates, and rather than having the mucus come into direct contact with all the airway cells going down to the alveoli, the way that this spreads is it goes from cell to cell.

The virus gets in there and it replicates, and then it releases enzymes, and then the cells begin to die. And those cells that die, the cell membrane breaks down and then they kind of coalesce, they congeal and they merge so that we have these big huge cells that have, they probably have five or six different nuclei in there, because these cells have merged, and that’s kind of the [syncytia 00:16:18]. The syncytia is kind of why we get the name respiratory syncytial virus. So it’s a cell to cell transmission, and this is fairly progressive. Again, takes a few days, and then this results in these cells dying, and then those little cells fall down the airway, and then they begin to occlude the airway and they ignite this massive inflammatory response. This results in increased mucus production, surfactant deactivation, edema, both interstitial edema and airway edema.

You can see here, based on this pathogenesis of RSV, that the cells are sloughing off, there’s increased mucus production, the cells migrate down through the airways, they create obstruction. So it’s a mixed bag in these patients, where you have airway obstruction in some of these lung units, and then you have atelectasis in others as a result of the obstruction or just by deactivation of the surfactant. But also through the inflammatory process. It’s like anything, you get inflammation in the lung, those are the kids you really don’t want to ventilate or expose to at least judicious levels of positive pressure. So the collapsed alveoli are a direct result of the obstruction, but also deactivation of the surfactant.

This is what the bronchial tubes look like under microscopy. You can see that there’s a number of alveoli that are inflated, but then the airways are extremely swollen. You can see that the airway lining is broken down. We have neutrophils and eosinophils that are occupying all of that air space, and then you’ve got these cells that slough off into the airway, and that’s what creates the airway obstruction as well as we’ve got mucosal edema here, with infiltrate of white blood cells. So this is not a homogenous disease, it’s a heterogeneous disease, and that’s why sometimes it can be difficult to treat these kids, especially when we’re mechanically ventilating. This is what a typical x-ray looks like in a child that’s affected with the whole bronchiolitis. This is just a kid with standard, straightforward obstructive bronchiolitis, not someone who’s impacted by the full on pneumonia that can be created by this disease. What we see here is an area of right up below the infiltrate. This is a focal area that is most likely result of alveoli that have collapsed as a result of a mucus plug. We can see here in the perihilar region that there’s a lot of kind of infiltrate, edema, inflammation, peribronchial cuffing, as a result of that interstitial edema in the large airways and in the vessels of the lung.

Now, if we were to get an x-ray a few hours later, we may find that that focal infiltrate has now migrated to here, or it’s migrated to here, and that these air bronchograms are better, or not, depending on our intervention. That’s why it has been suggested that we do not get serial x-rays in these kids. We’re exposing them to radiation and it doesn’t seem to really help these children, unless of course they get much sicker and they develop a severe pneumonia, and then we’re going to want to be able to get more x-rays in that case. But standard radiographic interventions are really not warranted in this case for these kids, mainly because it lags behind the clinical picture and presentation of the patient, but really doesn’t provide a lot of useful information about the therapy we provide.

However, and you look at the x-ray and you can say that’s subjective. We don’t have a lot of objective data to guide how we manage patients that are being supported with bronchiolitis. The one thing I can say though, however, is work of breathing, it’s a critically undervalued and underappreciated measurement in patients. In fact, we don’t really even know how to measure work of breathing, other than place an esophageal balloon catheter, which I’ll talk about a little bit later.

But work of breathing is something that all of us know. We know that if you work too hard, you’re most likely expending a lot of calories and your oxygen consumption is through the roof and your CO2 production, likewise, is kind of through the roof. We know that kids that are working harder are not necessarily getting better. And I think that the management of bronchiolitis really depends on evaluating work of breathing. That’s what helps guide us in our disease management. That’s what allows us to determine if a treatment is working, or if a baby’s responding to nasal suctioning versus nasopharyngeal suctioning. So we have to become experts, as therapists, as nurses, as doctors, on how to evaluate work of breathing.

With that being said, there really isn’t an awesome way to evaluate this. We actually have determined that we would like to look at modified asthma scores at our institution and look at inter-rater reliability. We show that that’s probably the best way to do it, and we can associate with these asthma scores, because we use them in our asthmatic patients. We’ve modified them a little bit to be able to work in our infant patients alike.

But if there is a better way to evaluate work of breathing out there that doesn’t include an invasive NAVA catheter, an invasive esophageal balloon catheter, then we’d love to hear about it. But for the most part, babies are going to generate a tremendous amount of interpleural pressure, especially in the case of severe disease, because they are trying to overcome the inelastic components of the lung, because we’ve got surfactant deficiency, we’ve got atelectasis, we’ve got patients who have to generate a high pleural pressure. And in doing so, they have to overcome the resistive elements of the lung. We know that if you have edema in the lung, if you have bronchoconstriction, and you have all of this secretion in the airway, and sloughed cells, these kids look horrendous. They typically are going to generate significantly high pleural pressures, to the point where their chest wall is going to collapse, their belly’s going to push up. As they get tired, their belly’s going to sink in a little bit more, and that’s a good indication that their diaphragm is starting to tire out. Babies don’t have a huge reserve, and so in that case, they’re going to be more sensitive to CO2 elevation and respiratory failure than we are. That’s why it’s especially important to evaluate their work of breathing, look at the intercostal retractions, look at the flaring of the nostrils. But also, in a baby who is grunting and head bobbing, that may indicate that they are not sufficiently maintaining enough back pressure in their lung and their lungs are collapsing. They’ve got mucus-filled lungs, and so if you’re nasal flaring, you’re grunting, and you’re head bobbing, that usually indicates that babies have more advanced respiratory failure.

At our institution, we monitor disease severity based more on this whole respiratory score, where we evaluate respiratory rate, we look at retractions, we look at dyspnea, or some surrogate of dyspnea based on shortness of breath. It’s not like these babies are telling us, “Hey, I’m short of breath,” especially since they’re less than two years of age. But we also include auscultation, and this score really consists of these four elements. The higher each of these individual things, the higher the score. And that prompts us to treat the patient more. So if we see that their score is higher, then we’re like, “Well, you know, yeah, I just went in, the nurse scored them, the respiratory therapist came in and scored this patient, the doctor did as well. We think it’s pretty high, so let’s, instead of doing nasal suctioning with an [olive 00:23:55] tip, let’s do nasopharyngeal suctioning, or let’s change our practice based on this.” And so we have a tendency to do the score, treat, score approach at our hospital.

So again, this was adapted from our asthma pathway. For whatever it’s worth, it seems to work for us. But if there are other validated scores out there that people are interested in sharing with us that take into account other things, we would love to hear from you.

So this is the respiratory score tool table, and as I mentioned before, you’ve got zero to three points, three being sicker, in patients based on normal respiratory rate and what we consider high respiratory rates in patients that are affected with this disease.

These are the retractions and the dyspnea and the auscultation. So these are the other three components of our respiratory score. So you get one point if you just have subcostal or intercostal retractions, but as you advance through and you start to get sicker, you’ve got the nasal flaring and the head bobbing, then we consider that a three. We look at dyspnea based on their ability to feed, their ability to vocalize. Obviously these kids are not going to be able to count to ten like they do in our asthmatic patients. We typically don’t include kids that are four years of age in our bronchiolitis pathway. We base it on feeding, vocalization, their ability to play, how interactive they are, versus patients who are super sick who just aren’t eating any more. Kids that are affected with this disease and have high work of breathing, they’re not going to want to eat. And that poses problems, which we’ll talk about here in just a little while.

So these are the components that make up our respiratory score. This is the pathway that we use. Again, this works for us, it may not be for everybody. But we include all kids that are less than two years of age. They may have viral symptoms, they may have lower respiratory symptoms. Nonetheless, they got admitted to our emergency room, or they got admitted to our ICU, and we have to work with them to determine ways in which we can reduce their work of breathing. Most of the time, these kids have increased cough, they have feeding difficulties. As I mentioned before, tachypnea, wheeze, low grade fever. If they have co-infection, then they’re likely to have a much higher fever. In that case, we do get a fair amount of kids who develop apnea. Apnea is, we’re not exactly sure why it happens, but it could happen as a result of nasal airway obstruction. It could also happen as a result of poor gas exchange in the lung. We’re not exactly sure, but that virus seems to cause babies to become apneic, and so obviously those kids are going to get admitted. They’re included in this strategy.

We do exclude kids with chronic lung disease and with cardiac disease, neuromuscular disease and immunodeficiency. Those kids are going to require something maybe a little bit different, especially if they’re requiring a home regimen or they’re on specific medications for their underlying cardiac disease. Those are kids that are at greatest risk, though, for developing severe forms of respiratory failure.

And also, we will include some of our ex-preemies that may not necessarily have chronic lung disease, but they are fairly young, and we just allow providers and we recognize the fact that these are the kids that are probably likely going to have more severe course of illness and may require escalating care.

So these are our admission criteria. If we’ve got a kid who’s come in through the ER and they have moderate to severe respiratory distress, and we have suctioned them, some of these kids come in on high-flow nasal cannula, and that’s a reason why they need to be admitted. A lot of them will be put on dry oxygen, and they’re not doing well with their saturations. We’ll admit those kids as well, but it’s really based on respiratory score. We consider hypoxemia at our institution as any oxygen saturation less than 90%, whether you’re on O2 or not, while awake, and then 88% while asleep. We try to get the pulse oximeter off as early as possible, because we realize that some babies just naturally are going to desat, and usually it’s self-resolving. Any kid that’s apneic, obviously we’re going to admit them. Dehydration is an issue, because if you’re not eating, and you’re not hydrating, then you’re not going to be able to mobilize the secretions very well. In those cases, if we’re not able to get an IV, or the kid is not eating, or not able to get NG hydration, that’s the number one reason why we would admit them.

We’ll admit them to the acute care floors for those reasons, but if we do start high flow nasal canula on these kids, we’ll directly admit them to the ICU. Especially if they’re an FI02 of 50 percent. If they have any lethargy, they’re not responding appropriately, they appear to have more obstructed airway disease, they look like they have kind of hypovolemia, apnea with bradycardia cyanosis, any of that, they go directly to the ICU. We’ll talk more about our bronchiolitis pathway here in a couple of slides.

But discharge, if we haven’t had to suction that kid for a number of hours, at least four hours, and the respiratory score is less than five, and they’ve been off oxygen for around 12 hours, there’s been no apnea, they’re starting to feed, all those things, then we’re more likely to discharge patients.

This is what our emergency room management guidelines look like. It’s kind of beyond the scope of this presentation to go through every aspect of our ED management, but again, these are our inclusion criteria, these are our exclusion criteria.

We do have an urgent care facility down the way, and so if kids are scoring greater than eight with a respiratory score, and they require more suctioning, and they’re not able to hydrate appropriately, then they will transport those kids to the hospital. Once they come in, obviously we place them in viral isolation.

We’re not gonna do an FA, we’re not gonna go in and try to figure out what the virus is unless we consider co-horting in this case. We may end up assessing what the cause of their viral pathogen is, especially if they get sicker, but it’s not standard. We don’t typically get x rays in this case. We try to focus on hydration, teaching the family, so that we can potentially get them out the door quicker and obviously suctioning them.

There are a large number of patients that get admitted to our emergency room primarily for the purpose of suctioning. Parents don’t have suction devices at home, or they have a bulb suction, which really isn’t that effective, so a lot of those kids will end up coming through the door, they get suction, then they get sent home. For the more severely ill patients, we have lots of really cool ways that we will intervene. We found, and I’ll emphasize this as we go through.

We found that rather than slapping a lot of these kids on high flow nasal cannula, we will take a different approach where we will suction them multiple times. We will score them, we’ll try to get antipyretics in to reduce their fever. We will try to hydrate them before we start the high flow, because we were starting a lot of them on high flow and there’s potential that you could forget about suctioning them as much because you’re trying to stabilize them on high flow.

We really try to suction as much as possible, do three rounds of suctioning and assess and evaluate based on their current O2 flow what their underlying respiratory status looks like. At that point we may consider doing high flow, and there’s certain guidelines for high flow, which I’ll talk about a little bit later.

We may suction these kids for upwards to one hour, and we’ll usually start with nasal suctioning. We won’t do nasal pharyngeal suctioning, and I’ll explain the reasons why we won’t do that from the beginning unless they start to develop more severe respiratory failure.

Then we have kind of admission criteria in those kids that aren’t really responding to what we’ve done. Then we have admission criteria for the acute care unit, and then we have ICU criteria admission as well. Just because we start a high flow nasal cannula trial, it doesn’t mean that we would send them directly to the ICU. We may actually admit them to the floor only as long as they’re clinically improving.

This is the acute care floor bronchiolitis patient protocol. It really emphasizes on the need for suctioning, and it’s all based on respiratory score where if your score is one to four, maybe we don’t have to do it as much. Maybe we suction nasally and do Q4. Whereas in patients that have high respiratory scores, maybe we suction them more frequently, upwards of Q1 hour. We use MP suctioning if the standard nasal suctioning isn’t working with olive tip. These are discharge criteria.

Over here I want to call out the therapies that are not routinely recommended. Albuterol, Racemic Epinephrine, Corticosteroids, chest PT, antibiotics, any of the mass cell stabilizers or hypertonic saline. All of those things, we don’t use those in the standard care of bronchiolitis patients. We reserve those for patients that are much sicker and we may or may not use some or all of these in that case.

I will mention also, that a lot of patients that are supported by bronchiolitis on the floor or the emergency room, by the time they get admitted to the intensive care unit we do not use these guidelines any longer. Things are going to change a little bit up there, and it’s likely that obviously their care is going to be a little more intensive and include some of the other therapies.

These are the treatments that work, and I think a large part for the reason why the cost of healthcare associated with bronchiolitis in the United States has to do with the fact that we like to do everything for these children when the only things that have high level evidence are going to be supplemental oxygen only if the kid is hypoxemic.

Suctioning, we’ve got to get the secretions that we have to alleviate the upper airway of the secretions and take the cells out and the mucus. Intravenous fluids, if you can’t get an IV, nasal gastric fluid administration is preferred. Only use these other therapies if there’s high risk. Those are the things. Suction, oxygen, fluids. Those are the things that really make a huge difference and those are the things we should really be emphasizing on. Again, we won’t give people oxygen in our institution unless they’re less than 90 percent.

If they’re asleep and they start to drop below 88 percent, then we’ll start to consider it but then we’ll look at the magnitude and the duration of the de-saturation’s. Some kids may go down to the eighties and that’s just what they do, but that doesn’t necessarily mean that you need to be chasing them, especially if they pop back up again and they’re able to resolve from their hypoxic or de-saturation’s.

What about other medical gases? I know that in some cases people want to be able to use Heliox gas, which is a resource that is slowly dwindling. I remember going to the store the other day with my daughter prior to a birthday party, and I wanted to be able to buy some helium balloons. Of course, you walk around the corner and they’re all trying to take the helium from the gas so they can laugh at each other with that high pitched voice. All they sell now is little balloons that are on a stick which give you kind of a false representation of a balloon floating up through the atmosphere. Heliox is not widely available now, and I know that people want to use this sometimes in bronchiolitic patients, because in those kids their work at breathing is super high because they have to generate this tremendous amount of transpulmonary pressure to get gas to move into the lungs.

What if we can provide a more laminar flow, what if we can reduce the resistance through the lungs and make it easier? I will say that there are some studies in mechanically ventilated patients and also in C-Pap that have demonstrated a reduced work of breathing, and have demonstrated reduced PACO2 values, and maybe that’s something that we use in high flow or we use in C-Pap, or we use it invasive patients. But for standard care of children, there really is no benefit in using Heliox, and it’s fairly expensive for the most part.

We have used it a few times and the studies that have been done, they’ve looked at modified respiratory scores, and they’ve demonstrated that some of these kids look better, but that doesn’t necessarily translate into improved outcomes for the patient especially when we consider length of stay, and keeping them out of the ICU. The verdict really isn’t in on this whole thing, and so if you use it, use it judiciously and make sure that you’re using a respiratory score to determine the effectiveness of this gas.

It’s tough to be able to use this with all of the available noninvasive devices, but it’s likely that we would want to use it with those over just giving it through a mask for some of these bronchiolitic patients. Also, it’s even more challenging to be able to provide that drug through a ventilator or C-PAP system. There’s only a few nowadays that are able to provide it without having your machine go completely haywire on you.

When it comes to blood gas monitoring, I don’t really know a lot of people that are looking at anything noninvasively other than saturations, and obviously people are looking at some of the end markers related to poor gas exchange which would include apnea, bradycardia, cyanosis. For the most part, we’re not drawing blood gasses on these kids unless they’re super sick.

If they have apnea, or they have lethargy, or they have poor profusion, or signs of impending respiratory failure, then we’re more likely to come in and do a capillary blood gas on these kids. For the most part, we like to look at pulse oximetry, and in fact pulse oximetry is probably one of the number one reasons why a kid would get admitted to the hospital because someone at an outside clinic, put them on a SAT monitor and their SATS are dropping below 90, and it freaks people out.

I think everybody has a SAT monitor nowadays. Again, that’s the number one reason why they get admitted to the hospital. Also, it is something that creates alarm fatigue, and it can cause caregiver distress. It probably pisses the families off. Most of these families that come in, they’re super tired, they’ve had the virus themselves for the last two weeks and they’ve got an alarm that’s going off nonstop. If they don’t have significant de-sats, it’s okay to take that SAT monitor off. Especially if their respiratory score is kind of in the five to six range or down to three or four.

The next thing we’re going to talk about is airway clearance. I think that all of us can kind of relate to this. I know that when I first became a respiratory therapist, I did more CPT, more albuterol treatments, and antiviral drug administration. We gave lots of treatments that obviously kept us busy, it kept us gainfully employed, but there was always a question in the back of my mind.

Are we impacting outcomes here? Is this really benefiting our patients? As time went on and there were more publications out there that demonstrated that albuterol simply probably doesn’t work in the majority of patients, airway clearance therapies like CPT probably don’t really provide much relief from this disease. You could be chasing your tail in those cases because you get an x-ray, you show a right upper lobe infiltrate, you do CPT there. Three hours later someone comes along, or a day later they get an x-ray and now it’s in the right lower lobe. You’re chasing your tail on those cases.

We try to reserve a lot of these advanced airway clearance treatments outside of suctioning for those kids that are sicker. These are our suctioning options right here. We have the bulb suction, we have the mouth operated nasal aspirator. You first. That’s not one that I’m going to be trying anytime soon, but I know that a lot of family members are trying that and they’re having fairly decent success where they’ll literally get on the other end of this and suck the secretions out of the nose. Hopefully they have a filter or tissue handy.

I’m okay with mucus and everything especially if it was my own kid, but again we’re not using these in the hospital setting. The ones that are really prevalent in the hospital setting is the olive tip suction, which really is kind of a noninvasive strategy where you just go in through the nose.

People may want to provide some saline in the contralateral there, or they put some saline in prior to going in and suctioning. Everyone swears that their method is better than the other. I like the one where they say that they put some saline in the contralateral there and suck through. But that’s not really widespread at our institution.

There’s a lot of speculation that we should be doing this, and not this, because this creates injury and inflammation and may further allow them to obstruct. Most people that swear by nasal pharyngeal suctioning. A lot of the respiratory therapists swear that by going down deep, you stimulate some of those pharyngeal and tracheal cough flexes, and that allows the kids that have more advanced disease to cough it up. Those thick secretions and we’re able to evacuate them.

Really, there’s no good data out there that supports using one over the other. There’s only data that actually shows that people who are being suctioned with nasal pharyngeal have a higher length of stay, and we don’t know if that’s because they’re sicker or the fact that we’re creating more inflammation in the airways.

We will reserve this one when this one isn’t working as well. Bulb suction is really not super effective because I don’t think it really provides enough negative pressure to be able to remove the secretions from the airways. Nonetheless, we have to get the secretions out.

If you reduce the airway resistance by a significant value, you reduce the work of breathing. Again, that’s our goal is that we want to be able to make it so that those secretions are not getting further down into the lung, and those secretions that are in there, we’re hydrating that patient appropriately and we’re able to get them out. That oftentimes requires the nasal pharyngeal suctioning.

Again, our strategy is respiratory, score, suction, score. We start with the nasal or the olive tip suction, and if the score remains around nine or greater, then we’ll do some MP suctioning. If it’s less than, maybe we will do one run of nasal pharyngeal suctioning to get a good suction and then we’ll put them on the supplemental oxygen and see how it goes from there.

Again, there are two articles now that support nasal pharyngeal suctioning is associated with increased length of stay, however using it less often does not make outcomes worse. Those two things really support using nasal suctioning over nasal pharyngeal suctioning. Other people may argue that’s not the case, and we shouldn’t really be basing our decisions on these two studies. We really don’t know.

I will say that the nurses are spectacular at Seattle Children’s Hospital. They are the ones that really guide this protocol a lot. We may go in and check on patients, especially if they’re on high flow nasal cannula or we may go in there and suction. The only time that they really call us to come down and suction is when they think that things aren’t going well.

The nurses are all trained on how to do nasal pharyngeal suctioning based on a job aid where they’ll go in and lubricate the airway, place it down based on the depth between the tragus and the nasal airway opening. Then they’ll suction on the way out. If they’re not able to remove those secretions effectively, then they call a respiratory therapist and we come down and try to intervene and see if we can suction a little bit deeper. The art or the practice of deep or nasal pharyngeal suctioning seems to be increasingly lost.

Because of that, we may see that some of these kids may need more intervention, and I say that based on my own experience. I actually spent the last two years in bronchiolitic patients’ rooms for several hours. We studied, we evaluated 16 patients that were supported with bronchiolitis and I worked with the nursing folks at Seattle Children’s Hospital. We all came together and we realized that there really wasn’t a lot of good high level evidence in the literature to support using these nasal pharyngeal suctioning over olive tip suctioning.

Really, what we wanted to do based on the AAP recommendation, where they basically can’t make a recommendation, is we want to be able to go in and look at these kids that are on the floor with varying levels of disease severity, and go in and compare changes in respiratory function between these two different nasal suctioning devices.

What we did, is we wanted to look at pulmonary regional ventilation distribution using a device that’s being designed and developed by Draeger Medical, which allows us to go in and map the distribution of tidal volume in the lung and determine prior to suctioning, and then at 10, 20, and 30 minutes. By removing secretions from the airway, how we’re able to better recruit the lung and provide better distribution of ventilation both at exhalation and during inhalation.

Also, we wanted to look at transcutaneous CO2, SPO2, and heart rate. And I thought this represented a very valuable situation for us to do research because again, there’s only really two or three papers out there and those papers are retrospective in nature. They’re not prospective, they don’t have a randomization strategy so we wanted to kind go in there and shed a little bit of light on these two suctioning techniques.

Our cohort of patients that we supported, this was a randomized crossover design so each of the babies that we took care of on the acute care floor, we went in and got consent on, each of those babies was supported or we provided suctioning with both nasal and nasal pharyngeal suctioning, and we randomized that order in which they received it, but they all received it. These were kids that were within our asthma pathway. These are all the inclusion and exclusion criteria.

This is the Draeger Pulmovista 500 device that is currently awaiting FDA approval in the United States. Draeger was gracious enough to loan this device to us. The way that it works is, if you look at this little image right here, it’s similar to looking at a CT scan slice, where you can look at the anterior and posterior or dorsal ventral aspect of the lung. Where you see dark is where there’s a lack of ventilation, but where you see white and you see blue, that represents optimal ventilation.

We can evaluate this breath by breath, but look at the inspired electrical impedance tomography, and look at the exhaled electrical impedance tomography to determine what our volumes are during inhalation and what our FRC is. It’s a surrogate of FRC from this slice of lung that we’re looking at. It’s a noninvasive procedure, it doesn’t expose the patient to any radiation. You basically place a series of electrodes all the way around the chest wall.

It injects a known voltage through these two electrodes here, and there’s a reference electrode here, and what it will do is it will look at that voltage as it goes through the chest and pick it up on the other side, and be able to determine through the whole chest what the impedance values are as a result of increasing airway resistance, increased aeration improvement, and compliance. In addition to this, we weighed the sputum prior to and following suctioning. We’ve weighed the sputum traps between olive tip and the nasal pharyngeal catheter. What we did find is that we had a two to two and a half fold increase in the amount of secretion weight. The amount of mucus was actually greater with the nasal pharyngeal catheter than it was with the olive tip, and I think a lot of that may have to do with the fact that you’re going down, you’re reaching further down into the airway, but also you’re stimulating a cough reflex. I think that was a pretty important finding.

Also, we’re in the process right now and later on this afternoon we learned about our statistical analysis on the study, but what we also are starting to show is that there is potential that the ventilation maybe improved with nasal pharyngeal suctioning. It may actually result in better end expository lung volumes than OT, but yet it’s too early for us to make that designation because we’re waiting on our statistics to come back.

You can see here at least in this one subject prior to any suctioning, you can see that there’s areas of darkness in here. They came along, they OT suctioned and in that 30 minutes you can see that it improved, but it didn’t improve as much as the nasal pharyngeal suctioning did in the same subject when we consider the pre suction versus post suction. We’ll find out. Hopefully this will shed a little bit of light on how we should be doing this.

What about CPT? I remember doing CPT on every single bronchiolitic patient regardless of whether or not they had an x-ray. There’s a Cochrane review, there’s other reviews that basically say the same thing. Based on fairly large numbers now, 12 randomized control trials, CPT did not decrease severity or time to recovery, duration of oxygen therapy, length of stay and parent’s impression of physiologic benefit.

So, it’s not routinely recommended and we don’t typically do it, especially in the routine treatment of patients with bronchiolitis. However, if we get kids that are sicker, we may consider it especially since you know they’re not coming off the ventilator.

You look at another systematic review that was published by the Respiratory Care Journal and a number of folks, and they looked at even larger number of patients which included subjects that had bronchiolitis and had pneumonia, so there was a fair number of pediatric subjects. Based on this data, they really couldn’t find any evidence that airway clearance, including CPT, improved oxygenation length of time on the ventilator, reduced stay in the ICU, any of these things.

People are starting to ask the question now similar to IPBB back in the day when I first started, is there really a clinical effect that we can appreciate from doing CPT? In some cases, especially in kids with pneumonia, it has been shown to actually increase the risks and may actually result in declining respiratory function. We really don’t know what the best thing to do is, but we just know that we probably don’t need to be doing this in everybody.

We hear a lot of people who are requesting airway clearance across the United States in bronchioles tics to prevent atelectasis. I can tell you firsthand that you can’t really prevent atelectasis with CPT unless you have significant mucus down there. The best way to really prevent atelectasis in these cases may actually be to suction them or to place them on CPAP or high flow nasal cannula.

Especially if they have an ineffective cough. We may obviously increase the frequency or switch over to NP suctioning, but if they have radiographic evidence, they have increasing FI02 requirements, there are secretions that we can’t suction out especially if they’re endotracheally intubated, then we’re most likely to do it in that case. That’s what makes their treatment intensive in the intensive care unit.

No one is going to argue that we may need to do that in those cases. For the most part, the take home message is that in the standard treatment of bronchiolitis, chest PT is really not warranted.

This is our airway clearance consult algorithm where at Seattle Children’s Hospital, the doctors enter an airway clearance consult order. Based on these indications, we will come in and we will determine based on these separate issues right here, what the patient would best benefit from.

Whether that’s a cough assist machine, or chest physiotherapy. I will say that it hasn’t really reduced our chest physio therapy, but it has reduced our chest physiotherapy in those kids that may have clear x-rays, or who have a strong productive cough. We try to emphasize and focus on the need to not provide CPT in kids that may have bronchiolitis just because we know that it’s not super useful unless they may be in the ICU. What about bronchodilators? This is another therapy I remember doing sometimes CPT and bronchodilators at the same time. I would be in a cohort room, this is back in my early twenties. I would literally spend hour upon hour in that room providing suctioning, bronchodilator, CPT.

I think the take home message when it comes to any aerosolized medication, is that there really isn’t a lot of good data to support doing it. In fact, there’s a fairly large number of infants that have been enrolled in this Cochran review that have said that there’s no real effectiveness related to bronchodilator as a result of decreasing hospital admission outpatient treatment.

You could argue that this is a relatively small sample size and that there’s no objective data, because we’re not in their measuring EIT. We’re not doing pulmonary function testing. Others may argue that the majority of the data that was published at the time used older nebulizers that may not be as efficient. I’m in that school.

Maybe the vibrating mesh nebulizer or if we looked at the PMDI with the new valve holding chambers, maybe there is an effect and we just under appreciating it at this point. But we really do reserve bronchodilators in those patients that need it the most. Because there’s such low-level evidence for supporting reducing the illness and the length of hospitalization, we realized that there’s side effects and there’s costs associated with this, and we may not use this routinely, obviously.

However, in those kids that do get sicker, then we will provide the drug, but we typically provide the drug with a PMDI with spacer, valved holding chamber. We won’t give nebulizers. It seems that the babies will tolerate the two puffs or the four puffs much better when it’s a short treatment time.

Otherwise, if you give the treatment with blow by, or with a mask, it seems to agitate them. These are very tired, very sick babies, so we will document the response in these kids, and if it’s not working then we won’t do it again unless it’s absolutely needed.

There’s other randomized controlled trials that have looked at the benefit of receiving epinephrine corticosteroids, antibiotics. Because of the low risks with coinfection, antibiotics really aren’t warranted. In fact, that’s part of the reason why we don’t get as many chest x-rays is because we don’t want to end up giving antibiotics for what we may believe as a right upper lobe pneumonia, when in fact it could just be some mucus plugging and distal atelectasis.

Any of these other antagonists agents, leukotriene receptor antagonists. There’s really no strong evidence to support doing any of these. There are some small studies especially in patients that are endotracheally intubated, that have demonstrated significant reduction in airway resistance as a result of Racemic epinephrine.

Racemic epinephrine actually seems to make a little more sense to me, because it has some of those bronchodilator properties, but also it gets in there and it has an effect on vasoconstriction, so it is able to cause vasoconstriction. And we know that these kids have a lot of airway inflammation. We’ll use albuterol initially. But then if they’re not responding, it’s not frequent, it’s not super common that we’ll give racemic, but we may consider it at some point.

Another relatively interesting aerosolized drug that may be beneficial in patients, in improving mucociliary clearance and elimination of secretions, is hypertonic saline. We know that it works pretty well on our CF patient population and so there’s lots of interest in these kids that have thick secretions as well. But the interesting thing over the last several years is that there really aren’t a lot of studies that support using this or even recommend this for routine use in patients. We will see some kids that get admitted to the Intensive Care Unit where we do give this, but there are risks with this as well. This has been shown to increase airway hypersensitivity, bronchoconstriction. And when you give this to a ventilator, even when you’re filtering it, there’s potential that you could get salt all over the expiratory valve. So there’s risks with all of that. And so again there isn’t a lot of evidence to support this.

There was a very recent study that was published that included a lot of patients admitted to the emergency room where clinicians and researchers treated them with back-to-back hypertonic saline treatments in kids with significant bronchiolitis and O2 requirements. And they compared those babies to ones that were given just normal saline, and the admission rate was not different between the two groups. In fact, there was more complications as a result of giving this in the Emergency Room with regard to cough and wheezing in patients.

So we’re not really sure who this would benefit. The sicker kids, how do we administer it? What is the cost benefit? And we need to kinda look at length of stay and hospital admission from the ER if we’re going to suggest this as widespread use. So when it comes to aerosol delivery, I will be giving another talk in October just specifically on aerosol delivery and some of the controversies that exist in aerosol delivery in neonatal and pediatric patients.

There really…when it comes to drug delivery there are multiple options. Everyone’s doing it a little bit differently. A lot of these kids are on high-flow nasal cannula so we often ask ourselves, “Well what’s the best way that we can do this? Do we do a blow-by? Do we take the cannula out? Do we use a PMVI with a spacer?” And to be quite frank with you, there isn’t a lot of definitive data out there to support one over the other. There are some studies using radio[inaudible 00:58:47]isotopes that have evaluated medication delivery between hood and mask in patients. So we have the Jet nebulizer with the mask. You can see that you get fairly decent deposition here but babies that are getting the mask are more likely to cry. And as you cry, you increase your flow and you get more impactive drug loss in the upper airway. And so it may be more beneficial to do hood or if you’re gonna do blow-by, which I would suggest not doing because it’s been shown to not really result in any drug delivery, but if you are doing that-hook a mask up to the end of the tube when you do your blow-by. ‘Cause that’s been shown to actually result in better drug delivery.

But if you can get the baby to cry by sitting with—laying with the mom, then your best bet at that point is to give either a Jet nebulizer with the face mask or a face mask with a PMVI with spacer. I would do the PMVI with spacer because it doesn’t chill the patients out. It doesn’t matter if they’re breathing in when you actualate the device because there’s a reservoir that’s valve. That’s mainly how we do it.

There’s tremendous interest in using high-flow nasal cannula because if we could integrate the nebulizer into the high-flow device then that would mean that we don’t have to take them off and run the risk of destabilization in those bronchiolitics that are supported by high-flow. So that’s preferred however you have to decrease your flow rate if you’re gonna do that. Some devices may not work as some high-flow systems may not work as well as others when you’re using nebulizer treatments. But the one thing I can say for sure is don’t take your treatment and put it over the high-flow nasal cannula because these are [inaudible 01:00:22]nasal breathers. There’s some good data out there that actually supports taking the cannula off and putting the treatment on and so I would support that definitely. And if you can’t do that then you’ve got to think about other options. So we’ll talk more about that in October during respiratory care week.

What about nasal CPAP? You’ve got a baby who’s got a plugged nose. Do we want to go in there and put a nasal…put binasal short prongs in there, provide CPAP either through a ventilator or bubble CPAP? These are bigger babies, so you may not be able to use bubble CPAP as well or an infant flow device. So it’s kind of tough to support babies with nasal CPAP that are bigger but most smaller babies there’s definitely significant benefit regarding improvement of alveolar recruitment. You want to get those small airways open. When you improve FRC and you improve lung volume, you improve the ability to propel those…that mucus and all that cellular debris forward because the baby can generate a more productive cough. And as you reduce the airway resistance, we know that this works well with BPD. We know it works well with RDS. We’ve learned a lot about that. But also in these kids with bronchiolitis. If you splint that airway open, in these kids who especially are gas trapping, then you’re able to get more of that gas out. You improve ventilation distribution, reduce the gas trapping, improve CO2. But furthermore, it has been shown to obviously improve the apnea that’s related to bronchiolitis. And again we’re not exactly clear why they’re apneic but we do know that especially with RSV, these kids are at an increase likelihood for developing that.

What is the quality of clinical evidence related to nasal CPAP? I intentionally put this slide in there. It’s a little blurry but that’s okay because this is a meta-analysis of all the clinical studies out there that have looked at outcomes like, they’ve looked at hospital admission. But most of these are short-term physiologic studies. Every one of these studies showed that when you compared the standard therapy with a oxygen cannula, that nasal CPAP, sure enough, it will reduce the work of breathing. It will improve ventilation. It will reduce the PACO2. But there really isn’t a lot of good high-level evidence to support using CPAP. But that doesn’t mean that you shouldn’t. And when you combine it with heliox it does show that you can improve work of breathing further and you can drive down the CO2 a little bit lower. So if you’re going to use this and you’re going to use it with heliox make sure that it’s a good device that you can use. We typically will use bubble because there’s no question that the flow going into that system is coming through a helium oxygen mixing device and we know what the mixture is coming in through there. But some devices won’t tolerate and will constantly alarm the use of heliox gasses.

So be careful when you’re doing that. But don’t exclude it. I wouldn’t say we can’t do CPAP. You can do CPAP. But you can also do other forms of noninvasive intermittent mandatory ventilation. Or high-flow nasal cannula which is what most people are doing.

And so this is a study that was super interesting that came out a few years back. When investigators in a subset of infants affected by bronchiolitis, they wanted to evaluate the effort or the work of breathing done by babies who were breathing spontaneously but also who were being supported by nasal CPAP. So by using an esophageal balloon catheter, we’re able to estimate pleural pressures. And so this is a patient who is breathing in and out, in and out. And that’s a pretty big pressure change. That’s negative ten that they’re breathing. But once they put them on to nasal CPAP of seven you can see that those pleural pressure changes were much lower. That means that these babies are able to maintain gas exchange. Breathing at not only a lower frequency but at less of an effort. That just kinda goes to show that nasal CPAP does work.

But what is the best nasal CPAP setting that we could be using? And we don’t really know but we can assume that it’s going to be five like we use in our NICU or six. But when we look at these babies, and we look at work of breathing between spontaneous breathing and then CPAP of four, seven, ten—we show that the work of breathing is actually lowest at a CPAP of seven. So that must be the magic number in this case for all ten subjects in reducing airway resistance and providing enough back pressure and humidity in the lung that we’re getting the secretions out and we’re able to ventilate more efficiently. It’s interesting that when we go up to CPAP of ten, our work of breathing starts to go up even higher. I think that is directly related to gas trapping. What we’re seeing here is more gas trapping. So I think CPAP of six, CPAP of seven probably is the sweet spot when considering CPAP for babies with bronchiolitis.

And one thing, I mean it’s not like we all have the ability to go into a room and place an esophageal balloon catheter and look at respiratory effort, but this is a score between no CPAP and CPAP. This is the modified Wood score I believe that people are using for bronchiolitis. You see that that score goes down significantly. It almost cuts in half in this case. And that correlates to a change in what we call pressure time product or the area under the curve for someone breathing in. And so their work of breathing is directly correlated to this Wood score. So I think as long as we have the ability to generate a score, not only should we be using that for suctioning, but we should use that for managing patients on CPAP and high-flow.

So this is a review of patients who were supported by nasal CPAP. Of those patients that were supported by nasal CPAP, at least several years ago, it showed that when they get to the Intensive Care Unit more than half of those babies are going to require invasive ventilation. If they got to that level, and they’re on CPAP, then they’re likely to require invasive ventilation. Whereas, if you look at babies who were supported with both nasal CPAP and IPPV, a lot of people are using NIPPV with a Rom cannula. Or they’re using the FlexiTrunk Fisher Paykel nasal mask or prongs through a ventilator. That doesn’t seem to have a huge impact on the reduction and the need for invasive ventilation. So once you do get to the ICU, and you’re using these forms of noninvasive support, the intubation requirement is fairly high. That was a number of years ago. I think the devices have improved; the interfaces have improved. And we have to kinda go back and kinda reiterate these studies and determine if there is some benefit at that point.

Now if you look at the comparison between high-flow nasal cannula and nasal CPAP, there are a number of studies that have also been published in looking at high-flow nasal cannula in those patients who are likely to go on to need invasive mechanical ventilation. The need for invasive ventilation has been shown to be much lower than the need for invasive ventilation with nasal CPAP or NIMV. And I’m not sure if that’s because these kids may have been treated with high-flow and then were put on CPAP or these were treated straight from the get-go. But one thing that I can say is that we have a tendency to kind of underappreciate the effects of high-flow nasal cannula which I’m going to get to in just a moment here.

So with regard to this whole NIV thing, I think we need to obviously investigate this a little bit better because the one study that has been published it not only included nasal CPAP babies but it included NIPPV—CPAP with a rate. Obviously they demonstrated that there’s less VAP. Obviously less need for antibiotics in those patients who were supported noninvasively. But there needed to be more studies that are directly focused on differences between nasal CPAP, high-flow, and NIV in patients with significant bronchiolitis. And I think in a large part the reason why we need to critically evaluate this is because we may support these kids for a long period of time on noninvasive support. That puts them at risk for developing pressure injuries as a result of having those in. Granted in RSV, we’re probably not supporting them as long as these preterm babies but like these preterm babies those kids with bronchiolitis are always at risk for developing some sort of pressure injury.

High-flow is something that really doesn’t necessarily result in pressure injury. I’m not going to say that we haven’t had kids that have had pressure injury, or that haven’t had pressure injury in our units because of high-flow, but it seems to be much less. And I think that high-flow, we don’t really give it as much consideration when we think about how much support is being created by high-flow nasal cannula. And we just kind of assume that it’s oxygen therapy, but it’s not.

I think that when we start to use flow rates that are greater than two liters a minute, we got to consider that this is a leaky system. However, we’re providing a monophasic flow down through the upper airway, through the dead space. And when they exhale through that monophasic flow which most do, especially if they’re babies and they’re obligate nasal breathers, and their tongue creates a natural seal, then we’re getting some back pressure. But we’re also eliminating CO2 rebreathing. So as we exhale, CO2 accumulates in the upper airway and we rebreathe that. And babies rebreathe more of that unfortunately than we do because their dead space is almost equal to the lung volume in some cases. So, proportionately, they have greater dead space and that’s why babies respond better to the whole heated high-flow CO2 elimination. And so it may be better tolerated than nasal CPAP because it’s an easier interface so as long as you’re using this to occlude only 50% of the nasal airway opening. And again this is fairly well documented that this creates less nasal airway injury. However, there aren’t a lot of studies.

We just completed one study that was published in the Respiratory Care Journal. And we evaluated in a spontaneously breathing model with 3D printed anatomic nasal airway models between low birth weight with a closed mouth, open mouth, term newborn all the way up to an adult. And what we found is that as you increase the flow rate, you provide more pressure at end exhalation that’s very similar in many ways to CPAP, and some devices provide more, may provide more, than others when we consider the internal tubing diameter and the size of the prongs, and so on and so forth. But when we look at those kids that maybe supported with bronchiolitis, depending on the device that you’re using if you’re using ten or even fifteen centimeters of water pressure upwards of twenty, you may be providing more pressure than you think. But also you’re driving the CO2 levels down.

We measured in the subject, or in the spontaneously breathing lung model, CO2 being bled into the lung model before the high-flow cannula was applied. And in these low birth weight babies you can see that we reduced CO2, end-tidal CO2. The reduction in CO2 increased as we increased the flow rate. And even in the term newborn and the toddler we were able to reduce that CO2 fairly significantly. You can’t do that with CPAP. You can do that with an I.V. But the question is are you synchronized? Are you not synchronized? It’s becoming more abundantly clear that in babies, especially, that high-flow nasal cannula may provide similar level of support as noninvasive positive pressure ventilation. We may actually look upon high-flow now as an intermediary form of support between CPAP and NIPPV.

There are clinical studies that actually demonstrate this. And we have to go back and kind of repeat some of the studies, knowing more about high-flow nasal cannula. This is a study that actually looked at the electrical impedance changes. So this would represent volume and then the darker would represent FRC of the baby who had bronchiolitis that was on standard oxygen cannula at less than two liters. And then when they applied the high-flow nasal cannula, you can see here that not only did the volumes increase proportionally, but the end expiratory lung volumes increased significantly by applying high-flow nasal cannula and then once the high-flow nasal cannula was removed. And I believe that was just four or six liters a minute. I’d have to go back and look but you can see that the lung volumes drop. So there is a benefit from that back pressure. And if you don’t think that there is then there’s certainly many different studies that will counter that and show that you can recruit the lung and that it does provide some pressure. But furthermore, unlike CPAP it’s gonna provide flushing of CO2 which is critical in some of these kids that have bronchiolitis.

This is a baby that we studied last winter. And this is a collaboration between Boston Children’s and Seattle Children’s Hospital where we evaluated at different flow rates in this one bronchiolitis patient the electrical impedance tomography. And you can see here that during inhalation and exhalation this looks fairly dark at two liters a minute high-flow. Now this kid could benefit from some CO2 flush and a little bit of back pressure. But as we increase that flow rate, you can see that this is whiter and it’s less dark in here. So if you think of this as a CT Scan, there’s greater distribution of volume within the lung and this kid obviously had a reduced respiratory rate, transcutaneous CO2. So there appears to be an effect as a result the high-flow nasal cannula. So if you’re not using it in bronchiolitis, it might be time to make a change.

There’s also some data out there showing that as you increase the flow rate, the work of breathing based on the pressure rate product which is going to be your esophageal pressure swing or pleural pressure swing times respiratory rate. When you use high-flow of five or even eight liters a minute, you start to approach the work of breathing that a baby, especially if they have bronchiolitis. It’s similar between the groups but maybe you’re not using this complex bonnet on their head. Rather you’re just using the higher-flow. And I think one of the beautiful things about high-flow nasal cannula is that you optimize humidity. And these babies obviously have dry desecrated airways and they may have been on dry, cold gasses for some time and that tends to dry the airway out and that does nothing for their mucociliary escalators so you have to apply heated humidified gasses and we know that high-flow is a wonderful way to do that.

We just don’t know what flow rate to be using and I know that we use flow rates that are probably a little bit lower than what others are using nationally. In this study, they used around 1.5 liters per kilo. Others are using two liters per kilo. That’s a pretty high flow and typically will limit ourselves at a max about 1.5 only because…

Whoops. Sorry about that. I’m going to go back to my…there we go. Back to my screen.

We limit ourselves to about 1.5 liters per kilo because based on our lung model findings that seems to be the appropriate back pressure in these cases. There are studies out there again that are retrospected by nature that have shown reduction in the need for invasive ventilation with high-flow nasal cannula. There needs to be more…there’s reductions in heart rate and respiratory rate. But when we look at the Cochrane metaanalysis (meta-analysis) and we look at the most recent studies that have been published to date, there’s really not a tremendous amount of evidence to support using this and that it’s even effective in babies with bronchiolitis. And just because there is kind of this absence of evidence it doesn’t mean that there’s evidence of absence. We’re going to use this but we’re going to try to use it appropriately.

And so short term studies obviously have shown that there’s improved gas exchange, reduced work of breathing. And outside the ICU, high-flow has been shown to reduce the need for escalation of care especially when you compare that to low-flow oxygen in a subset of patients that have higher respiratory scores. In the more recent study, comparing between high-flow nasal cannula and standard O2 administration, the length of O2 therapy wasn’t different. However this was a crossover study where the group as they got sicker on O2 cannula they were able to switch over to high-flow. So it’s tough to kind of interpret the results from this data but high-flow might be better. That’s kind of the conclusion. That high-flow may be better as a rescue therapy, so you could start with standard O2. This is the state-of-the-art of high-flow nasal cannula administration at our institution between 2013, 2014. These are the viral seasons right here. You can see that high-flow obviously results in these seasonal spikes where we were using a ton of it back in 2015. In fact, 10% of all patients that were admitted to our hospital in a 350 bed institution, which is growing, 35 to 40 units were being used. But we found that by changing our practice a little bit and not slapping everybody on high-flow but trying to maximize suctioning and get the secretions out before we actually start high-flow that it’s kind of gone down a little bit. But we still do use it quite a bit in our bronchiolitis patient population.

So these are our recommendations for high-flow. If you have a patient and they meet these criteria right here based on age and they are at a maximum flow of one, 1.5, or two liters for 30, 91, and six months, two years respectively. Then if they still have significant respiratory distress and they have hypoxia, then we need to potentially consider a trial of high-flow nasal cannula in these cases. We know that high-flow will reduce the work of breathing. It may potentially reduce the need for intubation. We know that intubation may not be a great thing in these kids. We want to be able to make sure that we suction, we hydrate these kids. We may consider albuterol once. We don’t have a lot of time to actually go through exactly what we do in our high-flow nasal cannula limb, but we obviously want to try to optimize M.P. suctioning. Consider the albuterol once if they’re super sick and then we would consider using high-flow. And these are our high-flow max settings for the floor and then these are the min settings for the floor.

So if we’re weaning between this, we don’t drop it by one liter a minute. We actually will assess and evaluate Q4 our need for reducing high-flow nasal cannula. But we would literally go from our floor minimum, or from our floor max to our floor minimum. Once we’ve reached that floor max, then they get sent to the ICU and they’re no longer part of our pathway.

I’ll make sure that I send these to all of you. Basically we have escalation pathways. If you’re FiO2 is greater than 50, you automatically go to the unit. We typically start the high-flow at room air and then we’ll start at the floor max. Then we’ll wean down from there. We could go from the floor max to nothing at all. We may not necessarily go to the minimum. But I don’t want to get beyond this and kind of get loss in the details of how we do this. But we have obviously very discreet or very focused weaning parameters in our patients and when we can determine whether they can start to eat again or if they get sicker these are the criteria for shipping off to the ICU.

So these are our flows in all the patients that would be supported by high-flow nasal cannula. It’s really based upon our high-flow nasal cannula protocol and the pressures that we measured in some of our 3D anatomic airway models. This is our escalation. Again, they’re off the pathway once they go to the ICU and then once they get to the ICU that’s when we may implement an I.V., or we may implement CPAP or may have to intubate them. Feeding practices—if we can get them down to that minimum floor setting then we may resume oral feeds. We obviously will place an NG tube if unable to feed.

One thing I will mention is that it’s absolutely critical, and I won’t get into a lot of invasive ’cause I know that we’re running out of time and many of you may have questions, but 25-60% of the patients admitted to the PICU may go on to develop acute lung injury. Sorry, acute lower respiratory infection, respiratory tract infection and need ventilation. Some of these kids end up on ECMO. Some of these kids end up on an invasive mechanical ventilator. They are very difficult to manage. And they can actually get sicker as a result of providing invasive mechanical ventilation. Luckily, with high- flow and CPAP we don’t have to intubate them as much. But we have to take into consideration the fact that mechanical ventilation can add insult to injury. It puts them at greater risk for developing hyperexpansion of the lungs and gas trapping. This is a patient that was gas trapping significantly. We’ve shown in studies that we aren’t able to trigger the ventilators well; but if you give albuterol or potentially go up on the PEEP setting, then you may be able to get the patient to trigger better because you’re reducing airway resistance. So I’m just going to kind of skip to prevention. I think as we move into this very, very busy viral season it’s very critically important that we take into account how this drug…or how this is being spread. Cover your mouth. Wash your hands. Educate the family. Take every little bit of information that I have provided today based on years of work and try to implement that in your practice. Let me know how I can help you guys ’cause ultimately I want to be able to help you improve the outcomes in your patients. So thank you for listening to me, and we have time for questions. Thank you.

Jeff Maglin: Thank you, Rob. That was excellent. Before we get to questions, and I know we only have a couple minutes left here, I just wanted to remind all attendees to look for the email with links to the CEU evaluation forms for you to complete and we’ll process the forms and generate certificates within a week. But I appreciate everybody joining the conference today or the webinar today and I especially want to thank Rob for an excellent presentation. Everybody, have a great rest of the week and please be on the lookout as we’ll have additional webinars coming up next month. Thanks again, Rob.